Cardiovascular
Emergencies and
12 Lead EKG’s
Condell Medical Center
EMS System
ECRN Packet
Module III 2007
Prepared by:
Sharon Hopkins, RN, BSN, EMT-P
Objectives
Upon successful completion of this
program, the ECRN should be able to:
–understand the normal anatomy &
physiology of the cardiovascular
system
–describe anatomical changes to the
heart during ischemic episodes
–differentiate presentations of patients
with cardiorespiratory complaints
–recognize ST elevation on
the 12 lead EKG
–identify and appropriately state
interventions for a variety of
dysrhythmias
–review discussion of case
presentations
–successfully complete the quiz with
a score of 80% or better
Cardiovascular System
 This
system is composed of the heart
and blood vessels
 Delivers oxygenated blood to all cells
 Transports hormones throughout the
body
 Transports waste products for waste
disposal
 The heart is a pump
–right pump is under low pressure
–left pump is under high pressure
3 Components of The
Circulatory System
Functioning heart
 Sufficient blood volume
 Intact blood vessels

If any one of the above 3 are not
working properly, the patient may be
symptomatic and could be in need of
intervention
Superior
vena cava
Right
atrium
Right
ventricle
Aorta
Left
atrium
Left
ventricle
Myocardial Blood Flow
 The
heart is a muscle (myocardium)
 3 layers
epicardium - smooth outer surface
myocardium - thick middle layer,
responsible for cardiac contraction activity
endocardium - innermost layer of thin
connective tissue
 Myocardial
blood flow
– via coronary arteries immediately off aorta
– heart is the 1st structure to receive
oxygenated blood - it’s that important!
Coronary Arteries
Left
main coronary artery
–left anterior descending coronary
artery (LAD)
supplies left ventricle, septum
–circumflex coronary artery
supplies left atrium, left
ventricle, septum, part of right
ventricle
Right coronary artery (RCA)
supplies right atrium & ventricle
Coronary Blood Flow
Collateral Circulation
 Development
of new blood vessels to
reroute blood flow around blockage
in a coronary artery
 New arteries may not be able to
supply enough oxygenated blood to
heart muscle in time of increased
demand
 Ischemia occurs when blood supply
to the heart is inadequate to meet
the demands
Influences of Heart Function
 Preload
– pressure under which a ventricle fills; volume
of blood returning to fill the heart
 Afterload
– the resistance the ventricle has to pump
against to eject blood out of the heart
– the higher the afterload the harder the
ventricle has to work
 Ejection
fraction (EF)
– percentage of blood pumped by the ventricle
with each contraction (healthy >55%)
– damage to heart muscle decreases EF
Influences On Preload &
Afterload
Preload
Afterload
 increased oxygen
 arteriosclerosis
demand increases
induced high B/P
volume of blood
can cause left
returning to heart
ventricle to
become exhausted
 temporarily not a
& stop working
problem
efficiently
 heart enlarges when
preload remains
increased (FrankStarling law)
Problems That Decrease
Ejection Fraction (EF)
 Myocardial
infarction (MI)
 Congestive heart failure (CHF)
 Coronary artery disease (CAD)
 Atrial fibrillation
 Cardiomyopathy
 Anemia
 Excess body weight
 Poorly controlled blood pressure
Coronary Artery Disease (CAD)
 Leading
cause of death in USA
– Narrowing or blockage in coronary artery
decreasing blood flow
– Atherosclerosis - thickening & hardening of
the arteries due to fatty deposits in vessels
– Plaque deposits build up in arteries
arteries narrow
arteries become blocked
blood clots form
 Overtime,
CAD can contribute to heart
failure & dysrhythmias
Coronary Artery Disease (CAD)
Plaque in a coronary artery breaks apart
causing blood clot to form and blocks artery
Symptoms of Cardiovascular
Problems
 Breathing
problems
– Shortness of breath (SOB)
– Paroxysmal nocturnal dyspnea (PND)
suddenly
awakens with
shortness of breath
–Orthopnea
dyspnea when lying down
–Breath sounds
are they clear or not clear?
 Peripheral
edema
–excess fluid found in tissues of the
most dependent part of the body
presacral
area in bedridden person
feet and ankles in someone up and about
 Syncope
–fainting when cardiac output falls
–fainting while lying down is considered
cardiac in nature until proven otherwise
 Palpitations
–sensation of fast or irregular heartbeat
 Pain
Initial Impression
 Not
necessarily important to know
exactly what to “name” the patient’s
problem (diagnosis)
 Important to identify signs and
symptoms that need to be treated
– think “what’s the worse case scenario?”
 Important
to recognize the possible
medical condition the signs and
symptoms may be representing
 Important to determine the right
treatment approach
Patient Assessment:
OPQRST of Pain Symptoms
 Onset
– Sudden or gradual?
– Anything like this before?
 Provocation
or palliation
– What makes it better/worse?
– What was the patient doing at the time?
 Quality
– What does it feel like (in patient’s own
words)?
 Radiation
– From where to where?
 Severity
– How bad is it on a scale of 0-10?
 Timing
– When did it start
– How long did it last?
– Continuous or intermittent?
Vital Signs: Tools for Pt Assessment
 Heart
rate
–too fast
ventricle
does not stay open long
enough to adequately fill
–too slow
rate
too slow to pump often enough to
maintain an adequate volume output
 Blood
pressure
–could be elevated in anxiety and pain
–low in shock
–serial readings (trending) tell much
 Respirations
– Abnormally fast, slow, labored, noisy?
Clear - hear breath sounds enter & exit
normal
Crackles - pop, snap, click, crackle
fluid in lower airways
Rhonchi - rattling sounds; resembles
snoring
mucus in the airways
Wheezes - whistling sound; initially
heard on exhalation
narrowing airways (ie: asthma)
Absence of sound - not good!!!
 Pulse
oximetry (SaO2)
–Measures percent of saturated
hemoglobin in arterial blood
–<95% indicates respiratory
compromise
–<90% indicates dire problem
–Need to evaluate reading with
patient’s clinical presentation do they match?
Inaccurate SaO2 Readings
Hypotensive or cold patient (falsely
low)
 Carbon monoxide poisoning (falsely
high)
 Abnormal hemoglobin (sickle-cell
disease) (falsely low)
 Incorrect probe placement (falsely low)
 Dark nail polish (falsely low)
 Anemia (falsely high - whatever
hemoglobin patient has is saturated)

 EKG
monitoring
– Indicates electrical activity of the heart
– Evaluate mechanical activity by measuring
pulse, heart rate and blood pressure
– Can indicate myocardial insult and location
 ischemia - initial insult; ST depression
 injury - prolonged myocardial hypoxia or
ischemia; ST elevation; injury reversible
 infarction - tissue death
–dead tissue no longer contracts
–amount of dead tissue directly relates
to degree of muscle impairment
–may show Q waves
ST depression
ST elevation
Q wave
Acute Coronary Syndrome
Variety of events that represent acute
myocardial ischemic pain (plaque rupture)
Unstable angina
Intermediate severity of disease between
stable angina and acute MI; tissue ischemia
Non-Q wave infarct (NSTEMI)
No ST elevation but MI is present with
tissue necrosis (death)
Q wave infarct (STEMI)
ST elevation MI with tissue necrosis (death)
Usually a large/significant infarct
Acute Myocardial Infarction
 Coronary
blood flow deprived so that
portion of muscle dies
– occlusion by a thrombus (blood clot
superimposed on ruptured plaque)
– spasm of coronary artery
– reduction in blood flow (shock,
arrhythmias, pulmonary embolism)
 Location
and size of infarct depends on
which coronary artery is blocked &
where
– left ventricle most common
AMI Signs & Symptoms
 Chest
pain - most common especially
in men
– lasts >15 minutes
– does not go away with rest
– typically felt beneath sternum
– typically described as heavy, squeezing,
crushing, tight
– can radiate down the arm (usually left),
fingers, jaw,upper back, epigastrium
 Pain
not influenced by coughing,
deep breathing, movement
Atypical AMI Signs & Symptoms
Persons with diabetes, elderly, women,
and heart transplant patients
 Atypical presentation - from drop in
cardiac output (CO)
– sudden dyspnea
– sudden lose of consciousness (syncope)
or near-syncope
– unexplained drop in blood pressure
– apparent stroke
– confusion
– generalized weakness
Atypical AMI Signs & Symptoms
 Women
at greater risk
– symptoms ignored (by patient & MD)
– under-recognized
– under-treated
 Typical
presentation in women
– nausea
– lightheadedness
– epigastric burning
– sudden onset weakness
– unexplained tiredness/weakness
Region X SOP Initial Treatment
Acute Coronary Syndrome
 Regardless
of the end diagnosis, all
patients treated initially the same
– IV-O2-monitor-vital signs-history
– aspirin
– nitroglycerin
– morphine if necessary
– 12 lead EKG obtained (transmitted to
ED by EMS)
 Treatment
fine-tuned as more
diagnostic information is obtained
Congestive Heart Failure
 Heart
unable to pump efficiently
 Blood backs up into systemic system,
pulmonary system or both
– Right heart failure
most often occurs due to left heart failure
can occur from pulmonary embolism
can occur from long-standing COPD (esp
chronic bronchitis)
– Left heart failure
most commonly from acute MI
also occurs due to chronic hypertension
Right Heart Failure
 Blood
backs up into systemic circulation
– gradual onset over days to weeks
– jugular vein distension (JVD)
– edema (most visible in dependent parts of
the body) from fluids pushed out of veins
– engorged, swollen liver due to edema
– right sided failure alone seldom a life
threatening situation
 Pre-hospital treatment most often
symptomatic
 More aggressive treatment needed when
accompanied with left heart failure
Left Sided Heart Failure
 Heart
unable to effectively pump
blood from pulmonary veins
 Blood backs up behind left ventricle
 Pulmonary veins engorged with blood
 Serum forced out of pulmonary
capillaries and into alveoli (air sacs)
 Serum mixes with air to produce
foam (pulmonary edema)
Progression Left Heart Failure
 Think
“left - lungs”
 Impaired oxygenation
– compensates by  respiratory rate
 Fluid
leaks into interstitial spaces
– auscultate crackles

interstitial pressure narrows bronchioles
– auscultate wheezing
 Dyspnea
& hypoxemiapanicrelease of
adrenalineincreased work load on heart
Left Heart Failure
 Sympathetic
nervous system response
– Peripheral vasoconstriction
peripheral resistance (afterload) increases
weakened heart has to pump harder to
eject blood out through narrowed vessels
blood pressure initially elevated to keep up
with the demands and to pump harder
against increased vessel resistance
diaphoretic, pale, cold skin
Asthma or Heart Failure?
Asthma
Left heart failure
 younger patient
 older patient
 hx of asthma
 poss hx heart problems
 unproductive cough  orthopnea
 meds for asthma
 recent rapid weight gain
 wheezing
 cough with watery or
foamy fluid
 accessory muscles
being used
 meds for heart problems
 wheezing
 JVD
 Pedal or sacral edema
Which Came First - CHF or AMI?
 Not
unusual to see the AMI patient in
pulmonary edema - watch for it!
 Often hard to determine which came first
and triggered the development of the
other problem
Heart failurepoor perfusion & hypoxemia
myocardium suffers from inadequate blood &
oxygen supplyacute myocardial
ischemiaacute coronary syndrome
AMIpoor pumping performance of
heartacute failure of left heart pumpleft
heart failure
Cardiogenic Shock
 Heart
extensively damaged; it can no
longer function as a pump
 25% of heart damage causes left
heart failure
 if >40% of the left ventricle is
infarcted, cardiogenic shock occurs
 High mortality rate
Signs & Symptoms
Cardiogenic Shock
 Altered
level of consciousness
– confusion to unconsciousness
 Restless,
anxious
 Massive peripheral vasoconstriction
– pale, cold skin, poor renal perfusion
 Pulse
rapid and thready
 Respirations rapid and shallow
 Falling blood pressure
Treatment Goals
Acute Coronary Syndrome
 Goals
– early recognition of a possible cardiac
problem
– minimize size of infarction
– reduce myocardial oxygen demand
– decrease patient’s fear & pain
(minimizes sympathetic discharge)
– salvage ischemic myocardium
– prevent development of dysrhythmias
– improve chances of survival
Region X SOP - Acute Coronary
Syndrome
 Oxygen
– may limit ischemic injury
 Aspirin
- 324 mg chewed
– blocks platelet aggregation (clumping)
to keep clot from getting bigger
– chewing breaks medication down faster
& allows for quicker absorption
– hold if patient allergic or for a reliable
patient that states they have taken
aspirin within last 24 hours
 Nitroglycerin
0.4 mg sl every 5 minutes
– dilates coronary vessels to relieve vasospams
– increases collateral blood flow
– dilates veins to reduce preload to reduce
workload of heart
– if pain persists after 2 doses, Morphine to be
started
 Morphine
- 2 mg slow IVP
– decreases pain & apprehension
– mild venodilator & arterial dilator
reduces preload and afterload
–2mg slow IVP repeated every 2 minutes
as needed, max total dose 10 mg
Treatment Goals
Congestive Heart Failure
 Goals
– improve oxygenation
– decrease workload of the heart
(ie: decrease preload & afterload)
Region X SOP
Treatment Stable Acute
Pulmonary Edema (B/P>100)
 Nitroglycerin
- 0.4 mg sl
– Vasodilator to create venous pooling
– Reduces preload & afterload
– Maximum 3 doses (repeated every 5
minutes if blood pressure remains >100)
 Consider
CPAP - use if indicated
Region X SOP cont’d
 Lasix
- 40 mg IVP
– Diuretic - excess fluid excreted via
kidneys
– Venodilating effect to pool venous blood
– Dose  to 80 mg IVP if patient on Lasix
at home
 Morphine
- 2 mg slow IVP
– Venodilator to increase pooling of blood
– Anxiolytic to calm anxious patient
– May repeat 2mg dose every 2 minutes
– Maximum total dose 10 mg
 Albuterol
- 2.5 mg/3ml nebulizer
– Wheezing may indicate
bronchoconstriction from excessive fluid
– Bronchodilator could be helpful
Region X SOP cont’d
 Hypotensive
side effects from
treatments used for stable
pulmonary edema
– Treatment used (NTG, Lasix, Morphine,
CPAP) can all cause venodilation  B/P
– Blood pressure needs to be carefully
monitored
Region x SOP
Treatment Unstable Acute
Pulmonary Edema (B/P<100)
 Contact
Medical Control
 CPAP on orders of Medical Control
 Consider Cardiogenic Shock Protocol
 If wheezing (indicating
bronchoconstriction), contact Medical
Control for Albuterol order
– if patient needs to be intubated, Albuterol to
be delivered via in-line
Treatment Goals
Cardiogenic Shock
 Goals
– Improve oxygenation
– Improve peripheral perfusion
– Avoid adding any workload to the heart
Region X SOP
Treatment Cardiogenic Shock
 Oxygen
via nonrebreather mask
– BVM if respirations ineffective
– Intubation may become necessary
 Positioning
– Supine if lungs are clear
– Head somewhat elevated if pulmonary
edema is present (semi-fowler’s)
 IV/IO
fluid challenge in 200ml
increments if lung sounds are clear
– The shock may include a hypovolemic
component
Treatment Cardiogenic Shock
 Cardiac
monitor
– Arrhythmias are likely
May cause hypotension decreasing cardiac
output
 Dopamine
Infusion - maintain B/P >100
– Effects dose related & dependent on clinical
condition of patient
–5 - 20 g/kg/min has beta influence on
the heart
Increases
contractility strength of heart
To a lesser degree increases heart rate
 Dopamine
cont’d
– Doses >20g/kg/min
Alpha stimulation predominate &
vasoconstriction my negatively affect
circulation
 Extravasation
- leaking out of vessels
– Can cause tissue necrosis
– IV infiltration reported to ED staff; document
 Dosing
- start at 5 g/kg/min
– Refer to table in SOP page 13 OR
– Take patient’s weight in pounds, take 1st 2
numbers, & subtract 2 (ie: 185 pounds:
18 - 2 = 16 gtts/min to start drip)
EKG Monitoring & 12 Lead EKG’s
 Goal
EKG monitoring
– Identify a disturbance in the normal cardiac
rhythm
– Arrhythmias caused by
Ischemia
Electrolyte imbalances
Disturbances or damage in electrical
conduction system
 Goal
of obtaining 12 lead EKG
– Early recognition Acute Coronary Syndrome
 Treat
clinical condition, not the monitor!
12 Lead EKG’s
 EMS
to transmit EKG to Medical
control when following the Acute
Coronary Syndrome SOP
 Many patients can be monitored by a
Lead II but not all patients need a 12
lead.
 Some patients experiencing angina
or an acute MI will not yet have any
EKG changes indicated on the 12
lead.
12 Lead Transmitted From The
Field
 ECRN
to complete the radio report
 ECRN immediately after radio report
to retrieve faxed copy of the field 12
lead EKG
 12 lead EKG to be immediately
presented to the ED physician
 12 lead EKG from EMS is to be
placed on the patient’s chart after
MD review
A normal EKG DOES
NOT necessarily
mean there is
nothing acute going
on!
Cardiac Conduction System
 SA
node - dominant pacemaker
– upper right atrium
– blood supply from RCA
 Internodal
pathways
– to spread electrical impulse thru-out atria
 AV
node in region of AV junction
– in 85-90% of people, blood supplied by
RCA to AV node
– in 10-15% of people, blood supplied by
left circumflex
Conduction System cont’d
 bundle
of His
 Right and left bundle branches
 Purkinje fibers - through ventricular
muscle

Changes in electrolyte concentrations
influence depolarization and
repolarization
sodium (Na+), potassium (K+),
calcium (Ca++), Magnesium (Mg++)
Conduction System
LLeft bundle
lbranches
EKG Wave Forms
P
wave
– depolarization of atria
 PR
interval
– depolarization of atria & delay at AV
junction
– normal PR interval 0.12 - 0.20 seconds
 QRS
complex
– depolarization of ventricles
– normal QRS complex <0.12 seconds
T
waves
– repolarization of ventricles (and atria)
The J Point
J point - end of QRS complex & beginning
of ST segment
 ST segment elevation - evaluated 0.04
seconds after J point

Precordial Chest Leads
For every person, each precordial lead
placed in the same relative position
 V1 - 4th intercostal space, R of sternum
 V2 - 4th intercostal space, L of sternum
 V4 - 5th intercostal space, midclavicular
 V3 - between V2 and V4, on 5th rib or in
5th intercostal space
 V5 - 5th intercostal space, anterior
axillary line
 V6 - 5th intercostal space, mid-axillary
Precordial
Leads
Lead Placement
 The
more accurate the lead
placement, the more accurate the
12-lead interpretation when
interpreted from all other EKG’s
taken on this patient
 12-leads are often evaluated on a
sequential basis, each interpretation
made trying to consider the previous
one
 V4-6 should be in a straight line
12 Lead Printout
 Standard
format 81/2 x 11 paper
 12 lead views printed on top half
I
aVR
V1
V4
II
aVL
V2
V5
III
aVF
V3
V6
 Additional single view of rhythm strips
usually printed on bottom of report
 Machines can analyze data obtained
but humans must interpret data
Limb Leads (Bipolar)
Lead I - views the
left (lateral) side of
heart
 Lead II - views the
bottom (inferior)
side of heart
 Lead III - another
inferior view of the
heart

I+
Limb Leads
(Unipolar)
 aVR
- view from
right arm
 aVL - lateral view
from left arm
 aVF - inferior
view from left leg
Precordial (Chest) Leads
Views the
septal,
anterior,
& lateral
portions
of the
heart
Heart in the Thoracic Cavity
Myocardial Insult
 Ischemia
– lack of oxygenation
– ST depression or T wave inversion
– permanent damage avoidable
 Injury
– prolonged ischemia
– ST elevation
– permanent damage avoidable
 Infarct
– death of myocardial tissue
– may have Q wave
Evolution of AMI
A - pre-infarct
B - Tall T wave
C - Tall T wave & ST
elevation
D - Elevated ST,
inverted T wave,
Q wave
E - Inverted T wave,
Q wave
F - Q wave
ST Depression
 Can
indicate
ischemia
electrolyte abnormality
rapid heart rate
digitalis influence
reciprocal changes to ST elevation
 ST
depression measurement
– 1 mm (1 small box) below baseline
measured 2 mm (2 small boxes) after
end of QRS
ST elevation
is more
significant so
should be
looked for in
opposite
leads when
depression
noted
T Wave Inversion
T wave represents ventricular repolarization
– Normally upright in all leads except V1 and aVR
Inverted T waves tend to represent
ischemia
Note
T wave
inversion
aVL,
V4 -6
ST Segment Elevation
 Myocardium
exposed to prolonged
hypoxia or ischemia
 Finding indicates injury or damage
 Injury probably due to occluded
coronary artery
 Muscle can still be salvaged
 If corrective intervention not taken in
timely manner, tissue necrosis/death is
likely (infarction)
TIME IS MUSCLE!
Significant ST Elevation
 ST
segment elevation measurement
– 0.04 seconds after J point
 ST
elevation
– > 1mm (1 small box) in 2 or more
contiguous chest leads (V1-V6)
– >1mm (1 small box) in 2 or more
anatomically contiguous leads
 Contiguous
lead
– limb leads that “look” at the same area
of the heart or are numerically
consecutive chest leads
Contiguous Leads
 Inferior
wall: II, III, avF
 Lateral wall: I, aVL, V5, V6
 Septum: V1 and V2
 Anterior wall: V3 and V4
 Posterior wall: V7-V9
(leads placed on the patient’s back
5th intercostal space creating a 15
lead EKG)
ST Segment Elevation


Coved
shape
usually
indicates
acute
injury
Concave
shape is
usually
benign if
patient is
asymptomatic
Groups of EKG Leads
 Inferior
wall - II, III, aVF
 Septal wall - V1, V2
 Anterior wall - V3, V4
 Lateral wall - I, aVL, V5, V6
 aVR
is not evaluated in typical groups
 Standard lead placement does not look
at posterior wall or right ventricle of
the heart - need special lead placement
for these views
Pathological Q Waves - Infarction
 Death
of tissue
 Pathological Q wave
–>0.04 seconds wide or
– 1/3 of R wave height
–when seen with ST elevation
indicates ongoing myocardial
infarction
 Remember: ST segment probably
single most important element on EKG
when looking for evidence of AMI
Pathological Q Wave
Reciprocal Changes
 Changes
seen in the wall of the heart
opposite the location of the infarction
 Observe ST segment depression
 Usually observed at the onset of
infarction
 Usually a short lived change
 Lead
Reciprocal changes
 II, III, aVF
I, aVL
 I, aVL, V5, V6
II, III, aVF
 V1-V4
V7-V9
Acute MI Locator Table
Location
Leads
Reciprocal
changes
Inferior
(RCA)
Septal
(LAD)
Anterior
(LAD)
Lateral
(Circumflex)
II, III, aVF
I, aVL
V1, V2
V3, V4
II, III, aVF
V5, V6, I,
aVL
II, III, aVF
Acute Myocardial Infarction
Acute myocardial infarction (AMI) is part of a
spectrum of disease known as acute coronary
syndrome (ACS)
 ACS
– Larger term to cover a group of clinical
syndromes compatible with acute myocardial
ischemia
– Chest pain is due to insufficient blood supply
to the heart muscle that results from
coronary artery disease (CAD)
– Clinical conditions include unstable angina to
non-Q wave MI and Q wave MI

Common Complications of AMI
 V1-2:
septal wall - infranodal
heartblock, BBB
 V3-4: anterior wall - LV dysfunction,
CHF, BBB, 3rd degree HB, PVC’s
 I, aVL, V5-6: lateral wall -LV
dysfunction, AV nodal block in some
 II, III, aVF: inferior & posterior wall
LV - hypotension, sensitivity to
Nitroglycerin & Morphine
Practice Identifying ST Segment
Elevation
> 1mm (1 small box) in 2 leads from any
group or 2 or more contiguous leads
(>2 mm (2 small boxes) in limb leads
considered alternative elevation by some)
measured 0.04 seconds after J point
Think Pattern Recognition
Inferior Wall MI
I
Lateral
aVR
V1
Septum
V4
Anterior
II
Inferior
aVL
Lateral
V2
Septum
V5
Lateral
III
Inferior
aVF
Inferior
V3
Anterior
V6
Lateral
Think Pattern Recognition
Lateral Wall MI
I
Lateral
aVR
V1
Septum
V4
Anterior
II
Inferior
aVL
Lateral
V2
Septum
V5
Lateral
III
Inferior
aVF
Inferior
V3
Anterior
V6
Lateral
Think Pattern Recognition
Anterior Wall MI
I
Lateral
aVR
V1
Septum
V4
Anterior
II
Inferior
aVL
Lateral
V2
Septum
V5
Lateral
III
Inferior
aVF
Inferior
V3
Anterior
V6
Lateral
Think Pattern Recognition
Septal Wall MI
I
Lateral
aVR
V1
Septum
V4
Anterior
II
Inferior
aVL
Lateral
V2
Septum
V5
Lateral
III
Inferior
aVF
Inferior
V3
Anterior
V6
Lateral
Test Yourself What pattern would indicate an
anterior/septal wall MI?
I
Lateral
aVR
V1
Septum
V4
Anterior
II
Inferior
aVL
Lateral
V2
Septum
V5
Lateral
III
Inferior
aVF
Inferior
V3
Anterior
V6
Lateral
Practice Identifying
Leads Showing ST
Elevation
Evaluate the top 3 rows of the
12-lead EKG
Answers follow the 12 lead
ST Elevation II, III, aVF
Inferior Wall Involvement
ST Elevation V5, V6, aVL - Lateral
ST Elevation V1-V4 - Ant/Septal
ST Elevation II, III, aVF, V6
Inferior & Lateral Wall
ST Elevation I, aVL, V2-6
ST Elevation II, III, aVF
Case Discussion #1
 66
year-old male presents with
“indigestion” for past 2 hours,
frequent belching, nausea, paleness,
diaphoresis, left arm discomfort
 Vital signs
– 102/76
 What
HR 98
RR 20
SaO2 98%
is your impression and what
initial treatment is indicated in the
prehospital setting?
Case #1
 Impression:
possible AMI (assume and
treat for the worse)
 SOP:
Acute Coronary Syndrome
 Prehospital treatment:
– IV-O2-monitor-pulse ox
– Vitals stable
– History unremarkable
– Aspirin chewed (any contraindications?)
– Nitroglycerin sl (ask about Viagra use)
– Morphine if pain unrelieved after 2 NTG
– 12 lead transmitted to ED for interpretation
Case #1 12-Lead
Case #1
 Impression
of 12 lead?
– no ST segment elevation noted
 Does
lack of ST segment elevation
change field treatment for this
patient?
– Normal EKG does not preclude that
acute myocardial event is occurring
– Acute Coronary Syndrome SOP to be
followed
Case Discussion #2
 77
year-old female with history of
CABG, hypertension,  cholesterol, and
long standing diabetes
 Presents with vague complaints of not
feeling well, very tired & no energy over
the last day
 Meds:
–Aspirin, Isoptin, Toprol,
Hydrochlorothiazide, Lipitor,
Glucophage
Case #2
 Vitals:
110/72 HR-72 RR-18 SaO2 97%
 Monitor (lead II rhythm strip):
Case #2
 What
is your initial impression?
 Need to at least consider possible MI
 Remember:
–women, elderly, and long standing
diabetics report the most atypical
complaints
 Remember:
–a lead II only looks at one view of
the heart
–a normal EKG does not rule out AMI
Case #2
 Prehospital
treatment:
–IV-O2-monitor (SR with PVCs)-vitals
–Aspirin appropriate?
–Nitroglycerin indicated?
–12 lead EKG necessary?
–What about antidysrhythmic for the
PVC’s?
call
Medical Control for guidance
oxygen is often enough to suppress
PVC activity
Case #2
 Aspirin
– if patient reliable and took own dose within
last 24 hours, can omit, document why
omitted and when taken
 Nitroglycerin
– patient not having chest pain. Defer to
Medical Control for orders
– no contraindications noted (B/P >100; no
viagra type drug used within past 24 hours
- ask, don’t assume!)
 12
lead should be obtained on high
index of suspicion
Case #3
 81
year-old female complaining of
shortness of breath for past 2 days.
Unable to tolerate lying flat; JVD noted
 History of CHF, angina, arthritis, and mild
COPD
 Vitals:126/92 HR-170 RR-24 SaO2 97%
 Medications: nitroglycerin PRN,
– Lasix 40 mg daily
– Potassium
– Aspirin, one daily
– Proventil inhaler PRN
Case #3 - What is this rhythm?
Check the rhythm strip on the bottom
 Rhythm
Case #3
Rapid atrial fibrillation
 Initial impression?
Rapid atrial fibrillation

heart rate  ineffective pumping 
 cardiac output
 Prehospital
treatment initiated
IV-O2-monitor-vitals-history
 Goal of therapy - slow down heart rate
 Is patient stable or unstable?
– Stable - B/P >100, alert & cooperative
Case #3
 Prehospital
ALS treatment
– If Diltiazem not available, then what?
 Verapamil
– 5 mg IVP slowly over 2 minutes
– If no response after 15 minutes and B/P
remains >100, repeat 5mg slow IVP
 Carefully
monitor patient for
development of further deterioration
and increased difficulty breathing
 Position of comfort - usually sitting up
Verapamil / Isoptin®
Action
 Calcium channel blocker
 Slows conduction thru AV node to
control ventricular rate
 Relaxes vascular smooth
muscle
 Dilates coronary arteries
Region X SOP - Verapamil
Indications
 Alternative to Diltiazem/cardizem
 SVT not responsive to 2 doses of
Adenosine - to terminate rhythm
 Stable rapid atrial flutter/fibrillation to control heart rate
Dosing
 5 mg IVP slowly over 2 minutes
 If no response after 15 minutes and
B/P >100, may repeat Verapamil 5 mg
IVP slowly over 2 minutes
Verapamil
Side Effects
 Headache, dizziness
  B/P from vasodilation
 nausea & vomiting
Contraindications
  B/P
 Wide complex tachycardias of uncertain
origin
 Heart block without implanted pacemaker
 WPW, short PR & sick sinus syndromes
Case #4
 32
year-old male patient with
complaints of chest tightness, shortness
of breath, and just not feeling well for
past 2 days. Also states sore throat and
ear pain. Very anxious & scared.
 No history, no meds
 Jogs 2-3 miles 5 times per week
 Vitals: 110/70 HR-68 RR-20 SaO2 98%
 Lungs clear; skin warm, dry & pink
Case #4
 Initial
impression
Cardiac?
Musculoskeletal (what has patient
been doing)?
Viral illness (sore throat & ear pain)?
 What treatment would EMS begin?
Cardiac - can give Aspirin but call
Medical Control for NTG or Morphine
Normal EKG cannot rule out ACS
process
Case #5
 68
year-old male called 911 due to
non-radiating chest discomfort (not
relieved with 3 of the patient’s own
nitroglycerin) with some minor
shortness of breath
 History:
– stable angina
– GERD
– hypertension (controlled with medications)
– Type II diabetic (recently diagnosed)
Case #5
 Allergies
- aspirin
 Medications
– nitroglycerin PRN
– isordil
– nexium
– verapamil
– glucophage
 Vital
signs
– 136/78 HR-78 RR-18 SaO2 99%
 What
is the initial impression & what
prehospital treatment is initiated?
Case #5
Initial impression: acute coronary syndrome
 IV-O2-monitor-SaO2-vitals & history
 Lead II EKG strip:


The patient in case #5 was just hooked up
for a 12-lead EKG when they grabbed their
chest and became unresponsive
Case #5
 What
is this rhythm strip?
 What
action needs to be taken by EMS?
Case #5 - VF
 Confirm
no breathing, no pulse
 Begin CPR until the defibrillator is ready
and is charged to maximum joules
 Clear the patient & deliver 1 shock
 Immediately resume CPR for 2 minutes
(5 cycles of 30:2)
 Check rhythm, defibrillate
 Meds: vasopressor (Epinephrine)
antidysrhythmic (choose 1)
 1 shock in between meds & 2 min CPR
VF/Pulseless VT SOP Meds
 Epinephrine
1mg every 3-5 minutes
IV/IO for duration of arrest
 Antidysrhythmic:
Amiodarone 300 mg IV/IO 1st dose
OR
Lidocaine 1.5 mg/kg IV/IO 1st dose
 Repeat dose antidysrhythmic x1 in 5 min:
If Amiodarone given, then 150 mg IV/IO
OR
If Lidocaine given, then 0.75 mg/kg IV/IO
Antidysrhythmics in VF/VT
 Amiodarone
to the vein)
needs to be diluted (irritable
– total of 20 ml syringe (med mixed with
saline)
– rapid push in VF/VT (slow if pt has pulse!)
 Lidocaine
-
– if unsuccessful defibrillation
contact Medical Control for 3rd dose order
– if defib successful & bolus given < 10 min,
begin drip 2mg/min (30 mcgtts)
– if defib successful & bolus given >10 min,
give Lido 0.75 mg/kg IV/IO & start drip
Case #5
The patient was defibrillated twice and
received 1 dose of epinephrine
 After the 3rd shock, 2 minutes of immediate
CPR resumed
 After 2 min of CPR, what is the rhythm?

Case #5
 Rhythm:
sinus rhythm
 EMS action?
– Determine if there is a pulse (yes!!!)
– Reevaluate airway, breathing, circulation-B/P
– Medications:
because no antidysrhythmic were given,
need to call Medical Control for direction
 if Lidocaine, usually 0.75 mg/kg IV/IO
 if Amiodarone, 150 mg diluted into 100 ml
bag D5W; run thru mini-drip tubing; run
piggyback at rapid drip over 10 minutes
May not want any antidysrhythmic given
ETT Route
 Endotracheal
tube route is
discouraged, not eliminated.
 Absorption found to be unpredictable
 ETT drugs if this route is used
L - Lidocaine
E- Epinephrine
A- Atropine
N - Narcan
 Double
the calculated amount for the
IV/IO route
Bibliography
 American
Heart Association Guidelines
CPR ECC 2005
 Beasley, B., West, M. Understanding 12Lead EKG. Pearson Ed, 2001.
 Caroline, Nancy. Emergency Care in The
Streets, Jones & Bartlett, 2008.
 Page, B. 12-Lead EKG, Pearson, 2005.
 Phalen, T, Aehlert, B. The 12-Lead EKG
in Acute Coronary Syndromes, 2006.
 www.clevelandclinic.org
 www.nhlbi.nih.gov/health/dci/Diseases